A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?
Article first published online: 25 DEC 2001
Journal of Internal Medicine
Volume 246, Issue 3, pages 247–252, September 1999
How to Cite
Andreev, E., Koopman, M. and Arisz, L. (1999), A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?. Journal of Internal Medicine, 246: 247–252. doi: 10.1046/j.1365-2796.1999.00515.x
- Issue published online: 25 DEC 2001
- Article first published online: 25 DEC 2001
- drug therapy;
- glomerular filtration rate;
- vitamin D
Abstract. Andreev E, Koopman M, Arisz L (Medical University-Sofia, Sofia, Bulgaria and University of Amsterdam, Amsterdam, The Netherlands). A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible? (Review.) J Intern Med 1999; 246: 247–252.
This is a review of the available information about drugs which cause an increase in plasma creatinine concentration without decreasing glomerular filtration rate (GFR). The GFR is the main, but not the single, determinant of the plasma creatinine levels. Several drugs, such as cimetidine, trimethoprim, corticosteroids, pyrimethamine, phenacemide, salicylates and active vitamin D metabolites, have been reported to increase plasma creatinine without influencing its glomerular filtration. Cimetidine, trimethoprim, pyrimethamine and salicylates can inhibit secretion of creatinine by the proximal tubule. Corticosteroids and vitamin D metabolites probably modify the production rate and the release of creatinine. The exact mechanism of phenacemide–creatinine interaction is not fully explained. These drug-induced alterations in plasma creatinine concentration have clinical significance when GFR is estimated by using plasma creatinine.